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(Stroke. 1999;30:546-549.)
© 1999 American Heart Association, Inc.

Original Contributions

Increased Platelet Activation in the Chronic Phase After Cerebral Ischemia and Intracerebral Hemorrhage

Fop van Kooten, MD; Giovanni Ciabattoni, MD; Peter J. Koudstaal, MD, PhD; Diederik W. J. Dippel, MD, PhD Carlo Patrono, MD

From the Department of Neurology, University Hospital Rotterdam (F. van K., P.J.K., D.W.J.D.), the Netherlands, and the Departments of Pharmacology, Catholic University School of Medicine (G.C.), Rome, and University of Chieti "G. D'Annunzio" (C.P.), Chieti, Italy.

Correspondence to Fop van Kooten, MD, Department of Neurology, University Hospital Rotterdam Dijkzigt, 40 Dr Molewaterplein, 3015 GD Rotterdam, Netherlands. E-mail vankooten{at}neuro.fgg.eur.nl

Background and Purpose—Enhanced thromboxane (TX) biosynthesis has previously been reported in the acute phase after ischemic stroke. We investigated whether enhanced urinary excretion of 11-dehydro-TXB₂, a noninvasive index of platelet activation, was present in the chronic phase after a transient ischemic attack (TIA) or stroke, including intracerebral hemorrhage.

Methods—We obtained a single urinary sample from 92 patients between 3 and 9 months after onset of stroke or TIA. The urinary excretion of the major enzymatic metabolite of TXA₂, 11-dehydro-TXB₂, was measured by a previously validated radioimmunoassay. The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases.

Results—Urinary 11-dehydro-TXB₂ averaged 294±139, 413±419, and 557±432 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracerebral hemorrhage, respectively; the values were higher in all subgroups (P<0.01) than that in control patients (119±66 pmol/mmol). Increased 11-dehydro-TXB₂ excretion was present in 59% of all patients, in 60% (P<0.001) of patients with TIA, in 56% (P<0.001) of patients with ischemic stroke, and in 73% (P<0.001) of patients with intracerebral hemorrhage. Atrial fibrillation, no aspirin use, and severity of symptoms at follow-up contributed independently to the level of 11-dehydro-TXB₂ excretion in a multiple linear regression analysis.

Conclusions—Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persistent platelet activation, which is associated with atrial fibrillation and poor stroke outcome, can be substantially suppressed by aspirin treatment.

Key Words: cerebral ischemia • intracerebral hemorrhage • platelet activation • thromboxanes

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